Autophagy, a highly conserved mechanism for cell survival, emerges as an important pathway in many biological processes and diseases conditions. Studies of cultured renal cells, human kidney tissues and experimental animal models implicate that autophagy regulation is the critical aspects in chronic kidney diseases (CKD). Here, we summarize the current studies on the role of autophagy in CKD. Unveiling the precise regulation mechanism of autophagy in CKD is essential for developing potential prevention, diagnostic and therapeutic targets of these sticky clinical challenges.
Inhibition of cellular autophagy in proximal tubular cells of the kidney in streptozotocin-diabetic and uninephrectomized rats
Cellular autophagy in proximal tubules of early diabetic rats following insulin treatment and islet transplantation
Inhibition and restimulation by insulin of cellular autophagy in distal tubular cells of the kidney in early diabetic rats
Prevalence of chronic kidney disease and decreased kidney function in the adult US population: Third National Health and Nutrition Examination Survey
In vivo analysis of autophagy in response to nutrient starvation using transgenic mice expressing a fluorescent autophagosome marker
Recent advances in understanding the malnutrition-inflammation-cachexia syndrome in chronic kidney disease patients: What is next?
Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice
Tubular overexpression of transforming growth factor-beta1 induces autophagy and fibrosis but not mesenchymal transition of renal epithelial cells
Proximal tubular injury and rapid formation of atubular glomeruli in mice with unilateral ureteral obstruction: a new look at an old model
Autophagy promotes intracellular degradation of type I collagen induced by transforming growth factor (TGF)-β1.
Autophagy and apoptosis in tubular cells following unilateral ureteral obstruction are associated with mitochondrial oxidative stress
How can erythropoeitin-stimulating agent use be reduced in chronic dialysis patients?: Can reduction of inflammation improve ESA dose response?
Receptor for advanced glycation end-products promotes premature senescence of proximal tubular epithelial cells via activation of endoplasmic reticulum stress-dependent p21 signaling
Role of endoplasmic reticulum stress in apoptosis of differentiated mouse podocytes induced by high glucose
Quality control autophagy degrades soluble ERAD-resistant conformers of the misfolded membrane protein GnRHR
Hyperphosphatemia induces protective autophagy in endothelial cells through the inhibition of Akt/mTOR signaling
Autophagy regulates TGF-β expression and suppresses kidney fibrosis induced by unilateral ureteral obstruction
Podocyte autophagic activity plays a protective role in renal injury and delays the progression of podocytopathies
Stress in the kidney is the road to pERdition: is endoplasmic reticulum stress a pathogenic mediator of diabetic nephropathy?
ER-phagy mediates selective degradation of endoplasmic reticulum independently of the core autophagy machinery
Single nucleotide polymorphisms in the D-loop region of mitochondrial DNA is associated with the kidney survival time in chronic kidney disease patients
Ursolic acid attenuates diabetic mesangial cell injury through the up-regulation of autophagy via miRNA-21/PTEN/Akt/mTOR suppression
Methodology used in studies reporting chronic kidney disease prevalence: a systematic literature review
Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells
The roles of oxidative stress, endoplasmic reticulum stress, and autophagy in aldosterone/mineralocorticoid receptor-induced podocyte injury
Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction
Atg5-mediated autophagy deficiency in proximal tubules promotes cell cycle G2/M arrest and renal fibrosis
A network-based variable selection approach for identification of modules and biomarker genes associated with end-stage kidney disease
Nifedipine Upregulates ATF6-α, Caspases -12, -3, and -7 Implicating Lipotoxicity-Associated Renal ER Stress
Autophagy & Model Organisms
Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms